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Incomplete KLK7 Secretion and Upregulated LEKTI Expression Underlie Hyperkeratotic Stratum Corneum in Atopic Dermatitis
Get PDFThis is an open access article under the CC BY-NC-ND license. (http://creativecommons.org/licenses/by-nc-nd/4.0/).Atopic dermatitis (AD) is a common inflammatory skin disorder. Chronic AD lesions present hyperkeratosis, indicating a disturbed desquamation process. KLK7 is a serine protease involved in the proteolysis of extracellular corneodesmosome components, including desmocollin 1 and corneodesmosin, which leads to desquamation. KLK7 is secreted by lamellar granules and upregulated in AD lesional skin. However, despite increased KLK7 protein levels, immunostaining and electron microscopy indicated numerous corneodesmosomes remaining in the uppermost layer of the stratum corneum from AD lesions. We aimed to clarify the discrepancy between KLK7 overexpression and retention of corneodesmosomes on AD corneocytes. Western blot analysis indicated abnormal corneodesmosin degradation patterns in stratum corneum from AD lesions. The KLK activity of tape-stripped corneocytes from AD lesions was not significantly elevated in in situ zymography, which was our new attempt to detect the protease activity more precisely than conventional assays. This ineffective KLK activation was associated with impaired KLK7 secretion from lamellar granules and increased expression of LEKTI in AD. Such imbalances in protease-protease inhibitor interactions could lead to abnormal proteolysis of corneodesmosomes and compact hyperkeratosis. Upregulated expression of LEKTI might be a compensatory mechanism to prevent further barrier dysfunction in AD
TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与
Get PDFTrpm7 is a divalent cation-permeable channel that has been reported to be involved in magnesium homeostasis as well as cellular adhesion and migration. We generated urothelium-specific Trpm7 knock-out (KO) mice to reveal the function of Trpm7 in vivo. A Trpm7 KO was induced by tamoxifen and was confirmed by genomic PCR and immunohistochemistry. By using patch clamp recordings in primary urothelial cells, we observed that Mg(2+)-inhibitable cation currents as well as acid-inducible currents were significantly smaller in Trpm7 KO urothelial cells than in cells from control mice. Assessment of voiding behavior indicated a significantly smaller voided volume in Trpm7 KO mice (mean voided volume 0.28 ± 0.08 g in KO mice and 0.36 ± 0.04 g in control mice, p < 0.05, n = 6-8). Histological analysis showed partial but substantial edema in the submucosal layer of Trpm7 KO mice, most likely due to inflammation. The expression of proinflammatory cytokines TNF-α and IL-1β was significantly higher in Trpm7 KO bladders than in controls. In transmission electron microscopic analysis, immature intercellular junctions were observed in Trpm7 KO urothelium but not in control mice. These results suggest that Trpm7 is involved in the formation of intercellular junctions in mouse urothelium. Immature intercellular junctions in Trpm7 knock-out mice might lead to a disruption of barrier function resulting in inflammation and hypersensitive bladder afferent nerves that may affect voiding behavior in vivo.博士（医学）旭川医科大
Review of “Echinococcus and Echinococcosis, Part A.” edited by R. C. Andrew Thompson, Alan J. Lymbery and Peter Deplazes
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Thompson RCA, Deplazes P, Lymbery AJ, Editors. Echinococcus and Echinococcosis, Part A. Volume 95, Advances in Parasitology 95. Academic Press; 2017. 525 pages, ISBN 978-0-12-8114711 (hardcover); 9780128114728 (eBook)
肺癌患者の中心静脈ポート抜去に対するベバシズマブ投与の影響
Get PDF肺癌や大腸癌,乳癌などの治療に用いられるベバシズマブ(Bev)はその作用機序から創治癒不全を誘発する.皮下埋め込み型中心静脈ポート(CVP)は薬剤投与や補液目的に留置されるが,合併症による抜去が問題となる.Bev投与やその他因子がポート抜去に影響するか検討した.2008年10月～2016年7月の進行・再発肺癌148例を対象とした.合併症による抜去は23例で,内訳は感染11例,創し開による露出10例,閉塞2例であった.若年,Bev投与でCVP抜去に至る例が多かった.CVP使用開始までの期間は抜去群10.0日,非抜去群13.3日であり,抜去群の方が短い傾向であった.術後200日でのCVP留置率はBev投与あり53.1%,なし93.4%であった.CVP留置の際は,Bev投与による抜去の危険性について説明し,CVP使用までの期間を長くとることで,抜去例を減少させられる可能性が示唆された
